Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, ROC.
Institute of Medicine, School of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC.
Protein Sci. 2024 Nov;33(11):e5199. doi: 10.1002/pro.5199.
Antizyme (AZ) is a regulatory protein that plays a crucial role in modulating the activity of ornithine decarboxylase (ODC), which is the initial and rate-limiting enzyme in the complex pathway of polyamine biosynthesis. AZ facilitates the swift degradation of ODC, thereby modulating the levels of cellular polyamines. This study unveils a new ubiquitin-independent mechanism for AZ degradation, emphasizing the essential role of N-terminal degrons. Contrary to traditional ubiquitin-dependent degradation, our findings reveal that AZ degradation is significantly influenced by its N-terminal region. By conducting a series of experiments, including in vitro degradation assays, cycloheximide chase experiments, differential scanning calorimetry, and measurement of cellular concentrations of polyamines, we demonstrate that N-terminal truncation significantly enhances AZ's stability and facilitates the reduction of polyamine levels by accelerating ODC degradation. The removal of the N-terminal portion of AZ results in a reduced degradation rate and enhanced thermal stability of the protein, leading to a more efficient inhibition of polyamine synthesis. These findings are corroborated by the analysis of AZ isoforms, AZ1, AZ2, and AZ3, which display differential degradation patterns based on the specific N-terminal segments. This substantiates a degradation mechanism driven by an intrinsically disordered N-terminal region acting as a degron, independent of lysine ubiquitination. These results underscore the significant regulatory function of the N-terminal domain in the activity of AZ and the maintenance of polyamine homeostasis.
抗酶(AZ)是一种调节蛋白,在调节鸟氨酸脱羧酶(ODC)的活性方面起着关键作用,ODC 是多胺生物合成复杂途径中的初始和限速酶。AZ 促进 ODC 的快速降解,从而调节细胞多胺的水平。本研究揭示了 AZ 降解的一种新的泛素非依赖性机制,强调了 N 末端降解部位的重要作用。与传统的泛素依赖性降解相反,我们的发现表明 AZ 降解显着受其 N 末端区域的影响。通过进行一系列实验,包括体外降解测定、环己酰亚胺追踪实验、差示扫描量热法和细胞内多胺浓度的测量,我们证明 N 末端截断显着增强了 AZ 的稳定性,并通过加速 ODC 降解促进多胺水平的降低。AZ 的 N 末端部分的去除导致降解速率降低和蛋白质热稳定性增强,从而更有效地抑制多胺合成。这些发现得到了 AZ 同工型 AZ1、AZ2 和 AZ3 的分析的证实,这些同工型根据特定的 N 末端片段显示出不同的降解模式。这证实了一种降解机制,该机制由作为降解部位的固有无序 N 末端区域驱动,与赖氨酸泛素化无关。这些结果强调了 N 末端结构域在 AZ 活性和多胺动态平衡维持中的重要调节功能。